Objectives: To determine the treatment effects produced in Class II patients by the Carriere® Motion 3D™ appliance (CMA) followed by full fixed appliances (FFA). Materials and Methods: This retrospective study evaluated 34 adolescents at three time points: T1 (pretreatment), T2 (removal of CMA), and T3 (posttreatment). The comparison group comprised 22 untreated Class II subjects analyzed at T1 and T3. Serial cephalograms were traced and digitized, and 12 skeletal and 6 dentoalveolar measures were compared. Results: Phase I with CMA lasted 5.2 ± 2.8 months; phase II with FFA lasted 13.0 ± 4.2 months. CMA treatment restricted the forward movement of the maxilla at point A. There was minimal effect on the sagittal position of the chin at pogonion. The Wits appraisal improved toward Class I by 2.1 mm during the CMA phase but not during FFA. Lower anterior facial height increased twice as much in the treatment group as in controls. A clockwise rotation (3.9°) of the functional occlusal plane in the treatment group occurred during phase I; a substantial rebound (−3.6°) occurred during phase II. Overjet and overbite improved during treatment, as did molar relationship; the lower incisors proclined (4.2°). Conclusions: The CMA appliance is an efficient and effective way of correcting Class II malocclusion. The changes were mainly dentoalveolar in nature, but some skeletal changes also occurred, particularly in the sagittal position of the maxilla and in the vertical dimension.

Squamous cell carcinoma of the head and neck (SCCHN) is an aggressive disease with poor patient survival. Galanin Receptor 2 (GALR2) is a G-protein coupled receptor (GPCR) that induces aggressive tumor growth in SCCHN. The objective of this study was to investigate the mechanism by which GALR2 promotes angiogenesis, a critical oncogenic phenotype required for tumor growth. The impact of GALR2 expression on secretion of pro-angiogenic cytokines in multiple SCCHN cell lines was investigated by ELISA and in-vitro angiogenesis assays. Chemical inhibitor and genetic knockdown strategies were used to understand the key regulators. The in-vivo impact of GALR2 on angiogenesis was investigated in mouse xenograft, chick chorioallantoic membrane (CAM) and the clinically-relevant mouse orthotopic floor-of-mouth models. GALR2 induced angiogenesis via p38-MAPK-mediated secretion of pro-angiogenic cytokines, VEGF and IL-6. Moreover, GALR2 activated small-GTP-protein, RAP1B, thereby inducing p38-mediated inactivation of tristetraprolin (TTP), which functions to destabilize cytokine transcripts. This resulted in enhanced secretion of pro-angiogenic cytokines and angiogenesis in-vitro and in-vivo. In SCCHN cells overexpressing GALR2, inactivation of TTP increased secretion of IL-6 and VEGF, whereas inhibition of p38 activated TTP and decreased cytokine secretion. Here we report that GALR2 stimulates tumor angiogenesis in SCCHN via p38-mediated inhibition of TTP with resultant enhanced cytokine secretion. Given that p38 inhibitors are in clinical use for inflammatory disorders, GALR2/p38-mediated cytokine secretion may be an excellent target for new adjuvant therapy in SCCHN.

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